Jorge A. Levisman

Cardiac effects of acute ethanol ingestion unmasked by autonomic blockade.

We assessed the effects of ethanol and autonomic blockade on left ventricular function in nine normal subjects, age 20-35 years, using M-mode echocardiography and systolic time intervals. On day 1, measurements were made of heart rate, mean velocity of circumferential fiber shortening, and left ventricular preejection period and left ventricular ejection time ratio (PEP/LVET), during a control period and after autonomic blockade. Autonomic blockade was produced with intravenous propranolol (0.2 mg/kg body weight) and atropine (0.04 mg/kg body weight). On day two, measurements were again made during a control period, then with ethanol alone, followed by addition of autonomic blockade to ethanol. One hundred eighty milliliters of ethanol were ingested over 60 minutes, resulting in a mean blood ethanol level of 110 mg/dl (range 77-135 mg/dl) at 60 minutes post-ingestion. There were no significant differences between the control data on days 1 and 2. Blood pressure was unchanged throughout the study. On day 1, autonomic blockade alone resulted in the expected increase in heart rate (p lt; 0.001), with a proportional increase in mean velocity of circumferential fibr shortening (p lt; 0.01), and an increase in PEP/LVET (p lt; 0.01). On day 2, ethanol alone resulted in no significant changes except for a slight increase in PEP/LVET (p lt; 0.02). Ethanol plus autonomic blockade, (day 2), compared with autonomic blockade alone (day 1), revealed a decrease in mean velocity of circumferential fiber shortening (p lt; 0.05), and an increase in PEP/LVET (p lt; 0.01), with a decrease in intrinsic heart rate (p lt; 0.001). We conclude that in normal subjects: 1) autonomic blockade does not directly affect contractility; 2) acute ethanol ingestion alone does not produce important changes in cardiac function; and, 3) ethanol in the autonomic blockaded heart causes a significant decrease in contractility. Thus, we infer that ethanol has a negative inotropic effect which is masked by catecholamines and/or autonomic nervous system discharge.

Echocardiographic diagnosis of a mobile, pedunculated tumor in the left ventricular cavity

A mobile left ventricular tumor was detected by echocardiography. The tracing showed a cluster of echoes in the left ventricular cavity corresponding to the location of the tumor as seen in angiograms. At surgery the tumor was attached to the interventricular septum by a thin fibrous stalk.

Posterior mitral leaflet motion in mitral stenosis.

A reduced rate of diastolic closure of the anterior mitral leaflet has been shown to occur in mitral stenosis, primary pulmonary hypertension, and in cases with reduced left ventricular compliance. Posterior notion of the posterior mitral leaflet in diastole has been the distinguishing feature to rule out the diagnosis of mitral stenosis. We have analyzed echocardiograms of 167 patients with mitral stenosis and have found 16 cases where the posterior mitral leaflet moved posteriorly, that is, in an opposite direction from the anterior mitral leaflet. Two other features were found that were helpful in establishing the diagnosis of mitral stenosis in these atypical cases, namely, thickening of the mitral leaflets and reduction or absence of the artrial wave.

Abnormal motion of the mitral valve with pericardial effusion: Pseudo-prolapse of the mitral valve

The echocardiograms of seven patients with large pericardial effusions were found to show posterior motion of the mitral leaflets in systole as seen in prolapse of the mitral valve. Repeat echocardiograms after resolution of the effusion revealed normal mitral valve motion. None of the patients had clinical evidence of prolapsed mitral valve. We postulate that a posterior swing of the heart within the pericardial fluid occurring in late systole causes posterior displacement of the mitral valve simulating a prolapsed valve.

Normal Posterior Mitral Leaflet Motion in Mitral Stenosis

In classical mitral stenosis (MS) a reduced early diastolic closing motion of the anterior mitral leaflet (AMD is associated with anterior motion of the posterior mitral leaflet (PML), parallel to AML, Reduced diastolic motion of AML is also caused by reduced left ventricular compliance or primary pulmonary hypertension. In these cases, however, the PML moves normally, posteriorly, away from the AML. Posterior motion of PLM has been used to exclude MS. We report 16 out of 167 cases of MS in whom the PML moved posteriorly in normal direction. In these cases, echocardiograohic diagnosis of MS was made by (a) thickening of the mitral leaflets and (b), reduction of absence of atrial wave of AML, when in sinus rhythm. The degree of MS or mitral insufficiency did not correlate with the direction of the PML motion. We suggest that the PML motion depends on the type of MS: Cuspul versus Commissural or Chordal. While in most cases the PML moves anteriorly, its posterior motion should not exclude MS.